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From association to function : MTNR1B

Bonnefond, Amélie (author)
Lille 2 University
Lyssenko, Valeriya (author)
Lund University,Lunds universitet,Genomik, diabetes och endokrinologi,Forskargrupper vid Lunds universitet,Genomics, Diabetes and Endocrinology,Lund University Research Groups,Steno Diabetes Center Copenhagen
 (creator_code:org_t)
2016-04-12
2016
English 19 s.
In: The Genetics of Type 2 Diabetes and Related Traits: Biology, Physiology and Translation. - Cham : Springer International Publishing. - 9783319015743 - 9783319015736 ; , s. 403-421
  • Book chapter (peer-reviewed)
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  • The discovery that variants in the melatonin receptor 2 (MTNR1B) gene were associated with glucose levels, insulin secretion, and risk for type 2 diabetes (T2D) in genome-wide association studies (GWAS) reinforced the previously suggested link between glucose homeostasis and circadian rhythmicity. Diurnal secretion of melatonin has reported to be altered in people with diabetes and rodent models of T2D. The proposed underlying mechanisms by which altered melatonin signaling could predispose to progression to T2D and gestational diabetes mellitus (GDM) involve altered expression of MTNR1B in pancreatic beta cells, leading to impaired insulin secretion, consequent increased fasting glucose concentrations, and eventually overt T2D. Thus blocking the inhibition of insulin secretion may have potential clinical implications, and these effects could be more pronounced in individuals carrying risk genotypes. Finally, given that melatonin could emerge as an attractive treatment for a variety of conditions including pregnancies associated with GDM, preeclampsia, and intrauterine growth retardation, pharmacogenetic studies are warranted to determine treatment response and side effects according to genotype.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)

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